EC (endothelial cell) responses to shear stress generated by vascular perfusion play an important role in circulatory homoeostasis, whereas abnormal responses are implicated in vascular diseases such as hypertension and atherosclerosis. ECs subjected to high shear stress in vitro alter their morphology, function and gene expression. The molecular basis for mechanotransduction of a shear stress signal, and the identity of the sensing mechanisms, remain unclear with many candidates under investigation. Translating these findings in vivo has proved difficult. The role of VEGF (vascular endothelial growth factor) flow-dependent nitric oxide release in remodelling skeletal muscle microcirculation is established for elevated (activity, dilatation) and reduced (overload, ischaemia) shear stress, although their temporal relationship to angiogenesis varies. It is clear that growth factor levels may offer only a permissive environment, and alteration of receptor levels may be a viable therapeutic target. Angiogenesis in vivo appears to be a graded phenomenon, and capillary regression on withdrawal of stimulus may be rapid. Combinations of physiological angiogenic stimuli appear not to be additive.
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December 2011
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Conference Article|
November 21 2011
In vivo shear stress response
Stuart Egginton
Stuart Egginton
1
1Angiogenesis Research Group, Centre for Cardiovascular Sciences, Medical School, University of Birmingham, Birmingham B15 2TT, U.K.
1email s.egginton@bham.ac.uk
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Publisher: Portland Press Ltd
Received:
August 18 2011
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2011 Biochemical Society
2011
Biochem Soc Trans (2011) 39 (6): 1633–1638.
Article history
Received:
August 18 2011
Citation
Stuart Egginton; In vivo shear stress response. Biochem Soc Trans 1 December 2011; 39 (6): 1633–1638. doi: https://doi.org/10.1042/BST20110715
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